Titin Transcripts in Thymomas

Skeie, Geir; Freiburg, Alexandra; Kolmerer, Bernhard; Labeit, Siegfried; Aarli, Johan A.; Appiah-Boadu, Samuel; Gilhus, Nils Erik

doi:10.1006/jaut.1997.0162

Cited by 22 publications

(24 citation statements)

References 29 publications

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“…Since titin antibodies are not usually found in early-onset MG patients, it is unlikely that their production is triggered by focal end-plate lysis caused by anti-AChR antibodies. Titin is expressed in both hyperplastic thymus and thymoma tissue, potentially providing a thymic site for primary autosensitization against titin antigens [81,82]. However, this does not explain the presence of anti-titin antibodies in late-onset MG patients without thymoma or their absence in patients with early-onset MG and thymic hyperplasia.…”

Section: Autoantibodies Directed Against Non-achr Skeletal Muscle Promentioning

confidence: 99%

Muscle autoantibodies in myasthenia gravis: beyond diagnosis?

Meriggioli¹,

Sanders

2012

Expert Review of Clinical Immunology

144

111

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Myasthenia gravis is an autoimmune disorder of the neuromuscular junction. A number of molecules, including ion channels and other proteins at the neuromuscular junction, may be targeted by autoantibodies leading to abnormal neuromuscular transmission. In approximately 85% of patients, autoantibodies, directed against the postsynaptic nicotinic acetylcholine receptor can be detected in the serum and confirm the diagnosis, but in general, do not precisely predict the degree of weakness or response to therapy. Antibodies to the muscle-specific tyrosine kinase are detected in approximately 50% of generalized myasthenia gravis patients who are seronegative for anti-acetylcholine receptor antibodies, and levels of anti-muscle-specific tyrosine kinase antibodies do appear to correlate with disease severity and treatment response. Antibodies to other muscle antigens may be found in the subsets of myasthenia gravis patients, potentially providing clinically useful diagnostic information, but their utility as relevant biomarkers (measures of disease state or response to treatment) is currently unclear.

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Section: Autoantibodies Directed Against Non-achr Skeletal Muscle Promentioning

confidence: 99%

Muscle autoantibodies in myasthenia gravis: beyond diagnosis?

Meriggioli¹,

Sanders

2012

Expert Review of Clinical Immunology

144

111

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“…Autoimmunity to the ryanodine receptor is also highly characteristic, but less frequent 57,77. A common theme shared by MG‐associated thymomas is the occurrence of mRNA coding for the autoantigens mentioned 78–80. Except for the cytokines, however, there appears to be an apparent lack of the respective proteins,77,81–84 although it is not excluded that translation into very small amounts of autoantigenic protein occurs, with potential implications for autoimmunization 85–88…”

Section: Pathogenic Concepts In Seropositive Mgmentioning

confidence: 99%

The Role of Thymomas in the Development of Myasthenia Gravis

Marx

Müller‐Hermelink

Ströbel

2003

Annals of the New York Academy of Sciences

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“…An active immunization against aberrantly expressed epitopes on neoplastic thymoma epithelial cells is probably the initiating event in thymoma-associated MG [56]. Titin epitopes and messenger RNAs (mRNAs) containing the MIR and N2-line regions of titin are expressed in neoplastic epithelial cells in thymomas [57]. Thymomas contain abundant cortical and maturing thymocytes in such an unorganized microenvironment that aberrant positive or negative selection of nascent T cells seems likely [58].…”

Section: Induction Of the Immune Response Against Titinmentioning

confidence: 99%

Skeletal muscle titin: physiology and pathophysiology

Go¹

2000

CMLS, Cell. Mol. Life Sci.

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Titins are a family of gigantic filamentous muscle proteins essential for muscle structure, function and development. Most of their sequence consists of repetitive modules of two superfamily motifs, immunoglobulin and fibronectin, interspersed with unique sequences. A special feature is that many regions are differentially expressed in different muscle types, providing unique characteristics. Titin is evolutionarily old, and many regions are highly conserved. Most mutations that alter titin's characteristics seem to be incompatible with life, since very few associated genetic diseases have been described. The autoimmune response against titin in the paraneoplastic form of myasthenia gravis is discussed.

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Titin Transcripts in Thymomas

Cited by 22 publications

References 29 publications

Muscle autoantibodies in myasthenia gravis: beyond diagnosis?

Muscle autoantibodies in myasthenia gravis: beyond diagnosis?

The Role of Thymomas in the Development of Myasthenia Gravis

Skeletal muscle titin: physiology and pathophysiology

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